Do depression, fatigue, and body esteem influence premenstrual symptoms in nursing students?

Purpose The purpose of this study was to investigate factors affecting premenstrual symptoms among nursing students, focusing on depression, fatigue, and body esteem. Methods The participants were 145 nursing students at a university located in Changwon, Korea. Data were collected from November 2 to November 30, 2019 using self-reported structured questionnaires, and analyzed using descriptive statistics, independent t-test, analysis of variance, Pearson correlation coefficients, and multiple regression analysis. Results The mean item score for premenstrual symptoms was 2.52±0.92, indicating a low level. The mean score for depression was 16.05±7.72, and 15.2% of participants were found to be moderately depressed and 9.7% severely depressed. The mean item score for fatigue was 4.84±0.84, indicating a moderate level, and body esteem was 2.94±0.44, indicating a moderate level. The premenstrual symptoms of nursing students showed a statistically significant correlation with depression (r=–.58, p<.001), fatigue (r=.33, p<.001), and body esteem (r=–.28, p<.001). Factors impacting premenstrual symptoms of nursing students were depression (β=.47, p<.001), dysmenorrhea (β=–.18, p=.009), menstrual cycle irregularity (β=.17, p=.013), and body esteem (β=–.14, p=.038). The total explanatory power of these variables was 41.0%. Conclusion Findings from this sample of nursing students suggest that intervention programs to relieve premenstrual symptoms should focus on depression, menstrual cycle regularity, dysmenorrhea, and body esteem

The Ministry of Education, and Human Resources Development

ABSTRACT Peroxisome proliferator-activated receptor (PPAR)-␥ and retinoic acid X receptor (RXR) heterodimer regulates cell growth and differentiation. Zinc finger transcription factor-9 (Zf9), whose phosphorylation promotes target genes, is a transcription factor essential for transactivation of the transforming growth factor (TGF)-␤1 gene. This study investigated whether activation of PPAR␥-RXR heterodimer inhibits TGF␤1 gene transcription and Zf9 phosphorylation and, if so, what signaling pathway regulates it. Either 15-deoxy-␦(12,14)-prostaglandin J 2 (PGJ 2 ) or 9-cis-retinoic acid (RA) treatment decreased the TGF␤1 mRNA level in L929 fibroblasts. PGJ 2 ϩ RA, compared with individual treatment alone, synergistically inhibited the TGF␤1 gene expression, which was abrogated by PPAR␥ antagonists. Likewise, PGJ 2 ϩ RA decreased luciferase expression from the TGF␤1 gene promoter. Promoter deletion analysis of the TGF␤1 gene revealed that pGL3-323 making up to Ϫ323-base pair region, but lacking PPAR-responsive elements, responded to PGJ 2 ϩ RA. PGJ 2 ϩ RA treatment inhibited the activity of p70 ribosomal S6 kinase-1 (S6K1), abolishing Zf9 phosphorylation at serine as did rapamycin [a mammalian target of rapamycin (mTOR) inhibitor]. Zf9 dephosphorylation by PGJ 2 ϩ RA was reversed by transfection of cells with the plasmid encoding constitutively active S6K1 (CA-S6K1). Transfection with dominant negative S6K1 inhibited the TGF␤1 gene. TGF␤1 gene repression by PGJ 2 ϩ RA was consistently antagonized by CA-S6K1. Ectopic expression of PPAR␥1 and RXR␣ repressed pGL3-323 transactivation with S6K1 inhibition, which was abrogated by CA-S6K1 transfection. PGJ 2 ϩ RA induced phosphatase and tensin homolog deleted on chromosome 10 (PTEN), whose overexpression repressed the TGF␤1 gene through S6K1 inhibition, decreasing extracellular signal-regulated kinase 1/2-90-kDa ribosomal S6 kinase 1 and Akt-mTOR phosphorylations. Data indicate that activation of PPAR␥-RXR heterodimer represses the TGF␤1 gene and induces Zf9 dephosphorylation via PTEN-mediated S6K1 inhibition, providing insight into pharmacological manipulation of the TGF␤1 gene regulation. The human transforming growth factor-␤ isoforms constitute extracellular signaling molecules that have antiproliferative effects on mammalian cells, promoting the expression of cell adhesion molecules and extracellular matrix proteins. In particular, transforming growth factor (TGF)-␤1 serves as a key fibrogenic mediator that can enhance extracellular matrix deposition and inhibit collagenase activity during fibrogenesis The peroxisome proliferator-activated receptors (PPARs) are transcription factors that are members of the nuclear This work was supported b

Dynamic left ventricular outflow tract obstruction without basal septal hypertrophy, caused by catecholamine therapy and volume depletion

Hypertrophic cardiomyopathy (HCM) with hypertrophy of the basal septum is the most common etiology of left ventricular outflow tract (LVOT) obstruction

Spontaneous Spinal Epidural Hematomas Associated With Acute Myocardial Infarction Treatment

Many studies have reported spontaneous spinal epidural hematoma (SSEH). Although most cases are idiopathic, several are associated with thrombolytic therapy or anticoagulants. We report a case of SSEH coincident with acute myocardial infarction (AMI), which caused serious neurological deficits. A 56 year old man presented with chest pain accompanied with back and neck pain, which was regarded as an atypical symptom of AMI. He was treated with nitroglycerin, aspirin, low molecular weight heparin, and clopidogrel. A spinal magnetic resonance image taken after paraplegia developed 3 days after the initial symptoms revealed an epidural hematoma at the cervical and thoracolumbar spine. Despite emergent decompressive surgery, paraplegia has not improved 7 months after surgery. A SSEH should be considered when patients complain of abrupt, strong, and non-traumatic back and neck pain, particularly if they have no spinal pain history

Taurine chloramine differentially inhibits matrix metalloproteinase 1 and 13 synthesis in interleukin-1β stimulated fibroblast-like synoviocytes

It has been suggested that taurine chloramine (TauCl) plays an important role in the downregulation of proinflammatory mediators. However, little is known about its effect on the expression of matrix metalloproteinases (MMPs). In this study, we investigated the effects of TauCl on synovial expression of MMPs. The effects of TauCl on MMP expression in IL-1β stimulated fibroblast-like synoviocytes (FLSs) were studied using the following techniques. Real-time PCR and semi-quantitative PCR were employed to analyze the mRNA expression of MMPs. ELISA was used to determine protein levels of MMPs. Western blot analyses were performed to analyze the mitogen-activated protein kinase and inhibitor of nuclear factor-κB (IκB) kinase signalling pathways. Finally, electrophoretic mobility shift assay and immunohistochemistry were used to assess localization of transcription factors. IL-1β increased the transcriptional and translational levels of MMP-1 and MMP-13 in rheumatoid arthritis FLSs, whereas the levels of MMP-2 and MMP-9 were unaffected. TauCl at a concentration of 400 to 600 μmol/l greatly inhibited the transcriptional and translational expression of MMP-13, but the expression of MMP-1 was significantly inhibited at 800 μmol/l. At a concentration of 600 μmol/l, TauCl did not significantly inhibit phosphorylation of mitogen-activated protein kinase or IκB degradation in IL-1β stimulated rheumatoid arthritis FLSs. The degradation of IκB was significantly inhibited at a TauCl concentration of 800 μmol/l. The inhibitory effect of TauCl on IκB degradation was confirmed by electrophoretic mobility shift assay and immunochemical staining for localization of nuclear factor-κB. TauCl differentially inhibits the expression of MMP-1 and MMP-13, and inhibits expression of MMP-1 primarily through the inhibition of IκB degradation, whereas it inhibits expression of MMP-13 through signalling pathways other than the IκB pathway

Intracisternal administration of NR2 subunit antagonists attenuates the nociceptive behavior and p-p38 MAPK expression produced by compression of the trigeminal nerve root

<p>Abstract</p> <p>Background</p> <p>We investigated the role of the central NMDA receptor NR2 subunits in the modulation of nociceptive behavior and p-p38 MAPK expression in a rat model with compression of the trigeminal nerve root. To address this possibility, changes in air-puff thresholds and pin-prick scores were determined following an intracisternal administration of NR2 subunit antagonists. We also examined effects of NR2 subunit antagonists on the p-p38 MAPK expression.</p> <p>Results</p> <p>Experiments were carried out using male Sprague-Dawley rats weighing (200-230 g). Compression of the trigeminal nerve root was performed under pentobarbital sodium (40 mg/kg) anesthesia. Compression of the trigeminal nerve root produced distinct nociceptive behavior such as mechanical allodynia and hyperalgesia. Intracisternal administration of 10 or 20 μg of D-AP5 significantly increased the air-puff threshold and decreased the pin-prick scores in a dose-dependent manner. The intracisternal administration of PPPA (1, 10 μg), or PPDA (5, 10 μg) increased the air-puff threshold and decreased the pin-prick scores ipsilateral as well as contralateral to the compression of the trigeminal root. Compression of the trigeminal nerve root upregulated the expression of p-p38 MAPK in the ipsilateral medullary dorsal horn which was diminished by D-AP5, PPPA, PPDA, but not Ro25-6981.</p> <p>Conclusions</p> <p>Our findings suggest that central NMDA receptor NR2 subunits play an important role in the central processing of trigeminal neuralgia-like nociception in rats with compression of the trigeminal nerve root. Our data further indicate that the targeted blockade of NR2 subunits is a potentially important new treatments strategy for trigeminal neuralgia-like nociception.</p

Genomic characterization of Nocardia seriolae strains isolated from diseased fish

Members of the genus Nocardia are widespread in diverse environments; a wide range of Nocardia species are known to cause nocardiosis in several animals, including cat, dog, fish, and humans. Of the pathogenic Nocardia species, N. seriolae is known to cause disease in cultured fish, resulting in major economic loss. We isolated two N. seriolae strains, CK‐14008 and EM15050, from diseased fish and sequenced their genomes using the PacBio sequencing platform. To identify their genomic features, we compared their genomes with those of other Nocardia species. Phylogenetic analysis showed that N. seriolae shares a common ancestor with a putative human pathogenic Nocardia species. Moreover, N. seriolae strains were phylogenetically divided into four clusters according to host fish families. Through genome comparison, we observed that the putative pathogenic Nocardia strains had additional genes for iron acquisition. Dozens of antibiotic resistance genes were detected in the genomes of N. seriolae strains; most of the antibiotics were involved in the inhibition of the biosynthesis of proteins or cell walls. Our results demonstrated the virulence features and antibiotic resistance of fish pathogenic N. seriolae strains at the genomic level. These results may be useful to develop strategies for the prevention of fish nocardiosis.

Association of the programmed cell death 1 (PDCD1) gene polymorphism with ankylosing spondylitis in the Korean population

The PD-1 (programmed death 1) molecule is a negative regulator of T cells. PDCD1 (programmed cell death 1) has been reported to have a genetic association in systemic lupus erythematosus and rheumatoid arthritis in Caucasians. However, there are no reports on the association between this gene and ankylosing spondylitis (AS). The present study investigated the association of the PD-1 polymorphisms and the haplotypes with AS in a Korean population sample. In a case-control association study, two single-nucleotide polymorphisms, PD-1.5 C/T and PD-1.9 T/C, were genotyped in 95 AS patients and 130 healthy controls. The T allele of the PD-1.9 polymorphism was more frequent in the Korean male population with AS than in the Korean male controls (21.0% versus 6.9%, odds ratio 1.89, 95% confidence interval 1.483 to 2.408). The frequency of the CT haplotype (PD-1.5 C/T and PD-1.9 T/C) was higher in the AS patients (19%) than the controls (5.4%) (odds ratio 1.83, 95% confidence interval 1.559 to 2.521). The PD-1 polymorphism was demonstrated in Korean AS patients. The results suggest a genetic association between the PD-1 polymorphism and susceptibility to AS